Purchase this article with an account.
Isabel J. Crane, Susan McKillop-Smith, Carol A. Wallace, Graeme R. Lamont, John V. Forrester; Expression of the Chemokines MIP-1α, MCP-1, and RANTES in Experimental Autoimmune Uveitis. Invest. Ophthalmol. Vis. Sci. 2001;42(7):1547-1552.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
purpose. To determine the location of the CC chemokines macrophage inflammatory
protein (MIP)-1α, monocyte chemoattractant protein (MCP)-1, and
regulated on activation of normal T-cell–expressed and secreted
(RANTES) during disease progression in experimental autoimmune uveitis
(EAU) and their relationship with the presence of the T helper cell
(Th)1–type cytokine IFNγ.
methods. EAU was induced by immunization of Lewis rats with retinal extract.
Consecutive cryostat sections were prepared from eyes at different
stages of EAU, graded for severity of uveitis and stained by using
antibodies to MCP-1, MIP-1α, and RANTES and to cell surface markers.
Supernatants from superficial cervical lymph node cells were examined
by ELISA for IFNγ, IL-4, and IL-10.
results. MIP-1α and IFNγ were present most frequently and most extensively
at peak disease but also were detectable in the choroid 8 days after
immunization, before clinical disease onset. MCP-1 and RANTES were
present at peak disease, but much less frequently. RANTES was
occasionally found in the choroid before clinical disease. By days 19
to 21 after immunization, although infiltrating cells were present,
there were only residual low levels of chemokine staining. MCP-1 and
RANTES were detected on CD3-positive cells and on some ED1-positive
cells, whereas MIP-1α was also associated with vessels and areas of
exudate. Lymph node cells cultured from animals with peak disease had
increased levels of IFNγ and IL-10, but for IFNγ this occurred only
after stimulation in vitro with retinal extract.
conclusions. Although MCP-1 and RANTES were associated predominantly with cells
infiltrating the retina, MIP-1α was also associated with resident
cells. All three are likely to exacerbate EAU—MIP-1α, to the
This PDF is available to Subscribers Only